Saudi Journal of Ophthalmology (2015) 29, 278286

Review Article

Advances in the treatment of central serous chorioretinopathy

Marwan A. Abouammoh, MD

Abstract

Central serous chorioretinopathy is a disease that is partly understood. Novel advancements have led to further understanding of
the disease, and have identified choroidal dysfunction as the principal element in CSCR development. New imaging tools have
aided in better monitoring disease response to various treatment models. Enhanced depth imaging optical coherence tomogra-
phy, in particular, has helped in observing choroidal thickness changes after various treatment models. To date, photodynamic
therapy and focal laser remain the main stay of treatment. More understanding of disease pathophysiology in the future will help
in determining the drug of choice and the best management option for such cases.

Keywords: CSCR, Central serous chorioretinopathy, Central serous retinopathy, Photodynamic therapy, Corticosteroids,
Treatment

! 2015 Production and hosting by Elsevier B.V. on behalf of Saudi Ophthalmological Society, King Saud University. This is an open
access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
http://dx.doi.org/10.1016/j.sjopt.2015.01.007

Introduction Clinical features

Central serous chorioretinopathy (CSCR) is an acquired
chorioretinal disorder that was first described by Von
Graefe in 1866 as recurrent central syphilitic retinitis.1
Other names used to describe this disease entity include
capillarospastic central retinitis, central angiospastic
retinopathy, central serous retinopathy, and central serous
pigment epitheliopathy.2,3
CSCR usually affects middle-aged men between the
ages of twenty and fifty years.46 It has also been associ-
ated with type A personality, or those who are experienc-
ing psychological stress.5,7 It has been also linked to use
of sympathomimetic agents, corticosteroid use in any
form, endogenous high levels of corticosteroids, and some
psychopharmacologic agents.813 Smokers tend to have
poorer vision and need longer period for visual
rehabilitation.14
Patients with CSCR most commonly complain of metamor-
phopsia, micropsia, blurred vision, and mild dyschromatopsia
in the affected eye. On fundus examination, typical signs
include a round well-demarcated detachment of the neu-
rosensory retina at the macula. Pigment epithelial detachment
(PED) of variable size can also occur and can be single or mul-
tiple. The subretinal fluid (SRF) can be clear or turbid/fibri-
nous. The turbid fluid may even form in the sub-retinal
pigment epithelial (sub-RPE) space.15,16 In chronic CSCR or
in patients with old resolved disease, RPE mottling, atrophy,
and clumping might be observed.1719 In addition, yellow dots
that are thought to represent phagocytosed photoreceptor
outer segments are frequently seen just over the inner surface
of the RPE.18 Other atypical CSCR presentations include bul-
lous neurosensory retinal detachment, inferior neurosensory
detachment with atrophic tracts, and multifocal CSCR.2,20,21

Received 27 October 2014; received in revised form 18 January 2015; accepted 19 January 2015; available online 24 January 2015.

King Saud University, Riyadh, Saudi Arabia

Address: Department of Ophthalmology, College of Medicine, King Saud University, P.O. Box 245, Riyadh 11411, Saudi Arabia. Tel.: +966
505476426; fax: +966 14775724.
e-mail address: dr.abouammoh@gmail.com

Peer review under responsibility Access this article online:

of Saudi Ophthalmological Society, www.saudiophthaljournal.com
King Saud University Production and hosting by Elsevier www.sciencedirect.com
Advances in the treatment of CSCR
Investigations for CSCR include fluorescein angiography
(FA) which may show ink blot pattern of leakage or the less
common smoke stack appearance that mimics a mushroom
cloud.22 In addition, dye pooling in the sub-RPE space can be
seen in cases of PED. Diffuse leakage or multiple leaking
points can be seen in recurrent, chronic, or multifocal CSCR.
Indocyanine green (ICG) angiography may demonstrate dilat-
ed choroidal vasculature corresponding to the site of CSCR
with choroidal hyperpermeability in the late phase.23,24 Opti-
cal Coherence Tomography (OCT) can demonstrate the neu-
rosensory detachment and areas of PED. Enhanced depth
imaging (EDI) OCT can show the thickened choroid in the
areas corresponding to the neurosensory detachment.25
Pathophysiology
Notwithstanding the well-identified clinical picture of
CSCR, its pathophysiology is inadequately understood. Pro-
posed theories include choroidal hyperpermeability which
overloads the RPE pumping mechanism responsible for
keeping the subretinal space dry and may in some
instances-lead to decompensation and SRF collection.8,26,27
RPE dysfunction is another theory for developing CSCR in
which focal damage of adjacent RPE cells or even a single
RPE cell leads to reversal of ion pumping mechanism and
resulting in fluid accumulation in the subretinal space.28,29
Marmor hypothesized that a dysfunction in the RPE metabol-
ic transport system is needed in order to accumulate subreti-
nal fluid in CSCR due to focal RPE defects.30
An alternative theory is a combined choroidal and RPE
dysfunction.31 In addition, there is a close relationship
between CSCR and both endogenous and exogenous corti-
costeroids suggesting a role in pathogenesis.912 It has been
suggested that corticosteroids might sensitize the choroidal
blood vessels or RPE to the effects of catecholamines;32 fur-
thermore, corticosteroids have certain genomic effects on
adrenergic receptor gene transcription and expression which
can result in an increase in the number of adrenergic
receptors.33,34
Zhao et al. were the first to demonstrate that blocking the
aldosterone upregulated the endothelial vasodilatory potas-
sium channels that prevented aldosterone-induced choroidal
thickening. This is suggestive of the presence of mineralocor-
ticoid receptors in the choroidal vasculature which might be
involved in the pathophysiology of CSCR.35
Treatment
CSCR is usually a self-limiting disease with spontaneous
resolution within 34 months with overall good visual out-
come.3638 However, recurrences are seen in up to 50% of
patients within the first year.39
Chronic CSCR diseases are the cases in which there are
diffuse RPE changes without evident detachment in most cas-
es.9 However it is sometimes difficult to clinically differentiate
a chronic disease from a recurrent episode of CSCR. Spaide
identified chronic CSCR as serous macular elevation detected
microscopically or by OCT, and is associated with RPE
atrophic areas and subtle leaks or ill-defined staining on
FA.15 These recurrences or chronic neurosensory detach-
ments may lead to RPE atrophy or hypertrophy with irre-
versible loss of visual function.4044
279
Given all of the above, observation can be regarded as a
first-line approach in newly diagnosed cases of less than
3 month duration.7 In addition, risk factors should be
addressed to increase the chance of spontaneous resolution.
This includes discontinuing exogenous corticosteroids intake
in any form if possible-, and life style modification for
patients with type A personality traits.7,9,10,4548 On the other
hand, different modalities of treatment for CSCR exist. These
treatments are reserved for chronic CSCR, recurrent CSCR,
single CSCR attack of more than 3 month duration, and if
the fellow eye suffered from permanent visual loss due to a
previous episode of CSCR whether acute or chronic. We will
discuss below, current, emerging, and advances in therapeu-
tics for CSCR.
Laser photocoagulation
Applying laser photocoagulation to the leaking RPE guid-
ed by FA has been shown to hasten resolution of the neu-
rosensory detachment in CSCR. Xenon laser was used at
first followed by krypton laser; currently argon laser is more
widely used.4951 Many level one evidence studies have
demonstrated faster resolution of SRF in patients who under-
went laser photocoagulation compared to control eyes.5254
Nevertheless laser photocoagulation does not influence the
final visual outcome or rate of recurrence.6,54,55
Therefore, argon laser photocoagulation is an effective
treatment for acute CSCR with clearly defined focal leakage
point as seen on FA given that the leakage is not subfoveal
or juxtafoveal. Still, side effects such as permanent scotoma,
laser scar enlargement, and laser induced CNV can still occur
(Fig. 1).
Micropulse diode laser photocoagulation
This method of treatment uses subthreshold diode laser
energy in order to minimize retinal damage. It is similarly
effective in CSCR with point source leakage but not in eyes
with diffuse leakage, and leaves no clinically detectable
laser-induced damage.5658 Since there is no visible endpoint
to diode micropulse laser (DMPL) application, ICG enhanced
DMPL can be used to identify treated areas with post-treat-
ment ICG angiography.59
To date, only one randomized clinical trial (RCT) assessed
DMPL versus argon laser photocoagulation in acute CSCR.60
Patients in both groups had complete resolution of SRF at
12 weeks of follow-up. All patients had no scotomas in the
DMPL group compared to 3 out of 15 patients in the argon
laser group who had persistent scotomas. Contrast sensitivity
was also significantly better in the DMPL group.60
Transpupillary thermotherapy
Transpupillary thermotherapy (TTT) is a 810 nm long-pulse
low-energy diode laser. It works by raising the temperature
of the choroid and outer retina while sparing the inner retina
and photoreceptors to some degree, but the exact mechan-
ism is not clear.61 First described in 2005 by Wei, short-term
encouraging visual and anatomical outcomes have been
observed in CSCR with subfoveal leaks, multiple or diffuse
leaks, and recurrent atypical CSCR with PEDs.6164 More well
structured RCTs with long-term results are required to estab-
lish the role of TTT in the treatment of CSCR.
280
Figure 1. Left eye of a 32-year-old man with chronic CSCR showing turbid subretinal fluid (top right). Fluorescein angiography shows pin-point leakage
between the optic nerve and fovea (top left). Six months after focal laser photocoagulation to the leakage site shows resolution of the subretinal fluid
with enlargement of the laser scar and some atrophic RPE changes (bottom right). Fluorescein angiography shows hypofluorescent area surrounded by a
hyperfluorescent rim corresponding to the laser scar (bottom left). (Courtesy of Dr. Saba Al-Rashaed).
Photodynamic therapy
Photodynamic therapy (PDT) with verteporfin has been
employed to treat both chronic and acute CSCR, as well as,
to reduce recurrences. It is believed that PDT works in CSCR
by inducing choroidal hypoperfusion, and vascular narrowing
and remodeling to negate choroidal hyperpermeability which
is consistently found in CSCR cases.65,66 Others have pro-
posed that PDT can also tighten the blood retina barrier.67
Standard PDT
Chan et al. reported the first case series of full dose, full
fluence PDT in 6 patients with persistent or chronic CSCR
with subfoveal leakage.68 Many RCTs demonstrated the effi-
cacy of PDT. Inoue et al. reported that PDT is not effective or
recurrence rate is thought to be high in eyes with no intense
hyperfluorescence on ICG.69 Moon et al. concluded that visu-
al recovery might be limited in CSCR patients with lengthy
symptom duration, post-PDT RPE atrophy progression, and
in patients with possible foveal injury from PDT.70 Tsakonas
and coworkers demonstrated the effectiveness and safety
of FA-guided full fluence PDT using multiple PDT spots at
the same session for chronic CSCR.71 Thus even FA-guided
PDT can be an effective alternative in cases where ICG is
not available.
Ruiz-Moreno treated 82 eyes with standard PDT for chron-
ic CSCR and showed that it can improve visual acuity and
reduce central macular thickness (CMT). SRF has disappeared
in all cases. In his large case series, no patient developed sev-
ere visual loss or complications derived from PDT with an
average follow-up of 12 months. However, 9 cases devel-
oped reactive RPE hypertrophy after PDT.72 Furthermore,
neuroretinal thinning after standard PDT has been described,
but is not correlated with visual acuity decrease.73,74 Morpho-
logical and functional chorioretinal changes such as RPE
M.A. Abouammoh
atrophy, external limiting membrane and inner segment/
outer segment junction line discontinuity have been
observed after standard PDT treatment for CSCR, but were
not correlated with the area of PDT treatment nor with the
change in visual acuity.74 These post-PDT changes probably
represent accelerated course of the disease, which if left to
its natural chronic course might cause more damage.
Due to possible treatment-related risks such as choroidal
ischemia, RPE atrophy, RPE rip, and secondary choroidal
neovascular membrane (CNVM), some safety measures were
adopted in order to minimize these risks.68,7578 These safety-
enhanced measures include reducing the dose or power (flu-
ence) of PDT (Figs. 2 and 3).
Reduced dose PDT
A short-term pilot study by Lai et al. using half dose verte-
porfin for chronic CSCR has demonstrated both efficacy and
safety.77 Chan et al. have shown in an RCT that included 63
patients that half dose PDT was also effective both
anatomically and functionally in treating acute symptomatic
CSCR.65 A comparative case series by Lim et al. have shown
that half dose PDT facilitated earlier resolution of SRF and
earlier recovery of visual function when compared to focal
laser. No difference in final functional and anatomical results
was noted at six month follow-up.79 Kim and coworkers used
FA-guided half dose PDT for acute CSCR and found that
long-term anatomic and functional outcomes were not con-
vincing when compared to observation only at the end of
one year of follow-up in spite of complete resolution of SRF
in 100% of cases at the 3 month follow-up point.80
Maruko et al. found that subfoveal choroidal thickness and
ICG hyperpermeability decreased after PDT compared to
laser photocoagulation.81 Ratanasukon et al. concluded that
about 45% of CSCR patients treated with half dose PDT
had photoreceptor disruption at 1-year follow-up that
Advances in the treatment of CSCR 281

Figure 2. Left eye of a 48-year-old man with recurrent CSCR who was misdiagnosed as wet macular degeneration. Note the dull foveal reflex and RPE
atrophic changes (top right). Fluorescein angiography shows diffuse irregular hyperfluorescence (top left). Optical coherence tomography shows shallow
subretinal fluid reaching the fovea (Down).

Figure 3. Indocyanine green of the previous patient in Fig. 2 shows dilated/engorged choroidal vessels corresponding to the leakage seen on
fluorescein angiography (top right). Late phase shows leakage from these choroidal vessels (top left). One month after half-dose photodynamic therapy
the hypocyanescent area corresponds to the site of treatment (bottom right). It shows overall reduction in vascularity with decrease in choroidal vessel
caliber. No more leakage can be seen on late phase of ICG (bottom left).

eventually led to poor visual outcomes. It should be noted,
however, that the photoreceptor line at baseline was difficult
to identify and that only the final photoreceptor status was
documented but was not compared to baseline photorecep-
tor status.82 Karakus et al. showed that half dose PDT was
effective and safe after up to 3 years of follow-up for chronic
CSCR with improvement in contrast sensitivity compared to
baseline.83
Dang et al. studied subfoveal choroidal thickness after
one-third PDT dose, and found that subfoveal choroid was
thicker in patients with acute CSCR than in normal population
with symptomatic eyes being significantly thicker than in fel-
282
low eyes.84 Zhao proposed that the lowest safe effective
dose of verteporfin was 30% of the standard dose in treating
acute CSCR.85 Uetani and colleagues showed that half dose
PDT was more effective than one-third PDT dose for chronic
CSCR.86 Nicolo concluded that chronic CSCR with posterior
retinal cystoid degeneration might do worse when treated
with half dose PDT when compared to chronic CSCR with
SRF alone.87
Reduced fluence PDT
As some of the risks of PDT still exist after reducing the
dose of verteporfin, reducing the fluence by decreasing laser
time or power was attempted. Reibaldi et al. compared full
fluence to half fluence PDT in chronic CSCR. Both treatments
achieved similar results in terms of visual outcome and SRF
resolution, but choriocapillaris ischemia was significantly
more in the full fluence group.76 Similar promising results
for reduced fluence PDT in terms of safety and efficacy have
also been documented with half fluence and even minimal
(12 J/cm2) fluence.8891
Ohkuma et al. concluded that the outer nuclear layer
thickness is a significant predictive factor for visual acuity
after reduced fluence PDT for CSCR at 1 year.92 Kang
et al. showed that subfoveal choroidal thickness decreased
after reduced fluence PDT, as well as, after spontaneous
resolution, but normal subfoveal thickness was only
achieved in the PDT group.93 Nicolo compared half-fluence
to half-dose PDT for chronic CSCR, and found that half-dose
PDT induced faster SRF resolution and that the effects seem
to last longer than half-fluence PDT. However, both were
equally safe.94
Larger RCTs with long-term follow-up are still needed to
establish the most effective and safe way for treating CSCR
using PDT. The ideal PDT treatment for CSCR would be that
which achieves the best results with the least possible
complications.
Intravitreal antivascular endothelial growth factor
(VEGF)
Attempts to treat acute and chronic CSCR with intravitre-
al bevacizumab are based on the hypothesis that choroidal
hyperpermeability is associated with increased expression of
VEGF, albeit high VEGF levels were not detected in the
aqueous humor.9598 Yet, Jung et al. have demonstrated
that CSCR patients who responded to intravitreal beva-
cizumab had higher aqueous levels than those who did
not respond.99
Lim et al. reported the absence of any positive effect in a
series of 12 patients treated with a single intravitreal beva-
cizumab injection (1.25 mg/0.05 ml) when compared to
observation group (12 eyes) during a six-month follow-up.
Bae et al. demonstrated in another RCT that reduced-fluence
PDT was superior to 3 monthly doses of intravitreal
ranibizumab. They found that over 1-year of follow-up, 16
eyes (89%) remained dry in the PDT group versus only 2 eyes
(12.5%) in the ranibizumab group. Visual acuity improved in
both groups, but the difference was significantly better in
the PDT group at the 3-month time point.100
Other uncontrolled case series suggest efficacy of anti-
VEGF intravitreal injections for CSCR both functionally and
anatomically.95,101107 As the natural history of CSCR is gen-
M.A. Abouammoh
erally favorable, the lack of controls in these case series, is
noteworthy. On the other hand, anti-VEGF therapy has a
much obvious, well-established role in CNVMs secondary to
CSCR.108,109
Anti-corticosteroids
The connotation of corticosteroid use and the develop-
ment of CSCR have led to the suggestion of anti-corticos-
teroids as a treatment.32 This has led to several clinical
trials to assess the effect of such treatment.
Ketoconazole is a synthetic imidazole which, in addition
to its anti-fungal properties, has anti-glucocorticoid effects
by blocking the conversion of cholesterol to androgenic glu-
cocorticoid end-products. Meyerle et al. did not note any
change in visual acuity, median lesion height on OCT, and
linear dimensions through an 8-week follow-up period for
5 chronic CSCR patients who received oral ketoconazole
600 mg per day for 4 weeks in spite of documented
decrease in endogenous cortisol levels.110 Golshahi in a
comparative non-randomized study of 15 patients with
acute CSCR treated with ketoconazole for 4 weeks versus
15 patients in the control group concluded that systemic
ketoconazole was not associated with a significantly better
outcome.111
Mifepristone (RU-486) is an abortifacient agent. Its
mechanism of action is mediated through its glucocorticoid
and progesterone receptor antagonistic effects. Nielsen
et al. studied 16 patients with chronic CSCR in an uncon-
trolled study. Systemic mifepristone 200 mg was adminis-
tered for up to 12 weeks. Seven patients gained P5 letters
of vision, and 7 patients had improved OCT findings. This
led to the conclusion that oral mifepristone has a beneficial
effect in some CSCR cases.112
Spironolactone and eplerenone are both aldosterone
antagonist agents. Spironolactone possesses additional
anti-androgen properties. Few case-series documented a
reduction or complete resolution of SRF level and significant
CMT reduction.113116 However, RCTs are warranted to fur-
ther clarify the role of aldosterone receptor antagonist in
CSCR. Currently there is only one ongoing trial with eplere-
none (Clinical trial: NCT01990677).
Rifampicin is an anti-tuberculous medication which is
thought to facilitate catabolism of endogenous steroids. It
causes a proliferation of the smooth endoplasmic reticulum
and an increase in the cytochrome P-450 content in the liver,
thus affecting the metabolism and bioavailability of endoge-
nous corticosteroids, consequently aiding in resolution of
CSCR and improving its symptomatology.117,118 However,
care is to be taken as hepatotoxicity can develop as a side
effect while being treated for CSCR.119
Finasteride is a weak anti-androgen that worked mainly
through inhibiting type II 5 a-reductase that is necessary for
converting testosterone to dihydrotestosterone (DHT), a
potent androgen. Forooghian et al. described 5 cases of
chronic CSCR treated with oral finasteride 5 mg daily for
3 months. Mean CMT and SRF volume decreased in all
patients. This reduction corresponded to a drop in DHT
serum levels in all patients. Following the cessation of finas-
teride, all patients but one had SRF recollection and an
increase in CMT.120 More trials are needed to evaluate the
effect of finasteride in CSCR.
Advances in the treatment of CSCR
Adrenergic blockers
As CSCR is closely associated with type A personality
which is characterized by high adrenergic activity, it was pro-
posed that blocking adrenergic receptors might have a posi-
tive effect on CSCR.121 It has been shown that CSCR patients
who were diagnosed to have hypertension and were started
on metoprolol a beta blocker had improved symptoma-
tology. Recurrence of CSCR once metoprolol was stopped
was also noticed.122 Chrapek et al. demonstrated no effect
of metipranolol on acute CSCR in a recent double-blinded
RCT in which 23 patients received 10 mg of metipranolol
for up to 45 weeks compared to placebo pills in 25
patients.123 The contradictory results demand further assess-
ment of the actual role of adrenergic blockers.
Systemic carbonic anhydrase inhibitors (CAIs)
CAIs are thought to mediate its action by inhibiting car-
bonic anhydrase enzyme in RPE, which supposedly aid in
SRF absorption. Pikkel et al. reported a prospective non-ran-
domized trial on 15 CAI-treated patients against 7 controls.
They found that oral acetazolamide shortens the time for
subjective and clinical improvement, but there was no differ-
ence in final visual acuity or recurrence rate between the two
groups.124
Aspirin
Caccavale et al. compared 109 patients with CSCR, who
were treated with aspirin 100 mg once a day for a month fol-
lowed by 100 mg every other day for 5 months, to a historic
control group of 89 patients. They concluded that treatment
with aspirin may hasten visual improvement and reduce
recurrences compared to no treatment.125,126 They theorized
that the CSCR is due to impaired fibrinolysis and increased
platelet aggregation in the choriocapillaris.125 Therefore, it
is presumed that aspirin works in such cases through its fibri-
nolytic and anti-platelet action.
Helicobacter pylori treatment
H. Pylori infection has been recently linked to CSCR.127,128
Rahbani-Nobar showed on a non-randomized trial the effica-
cy of anti-H. Pylori treatment regimen in hastening the
absorption of SRF.129 A RCT by Dang et al. concluded that
anti-H. Pylori treatment regimen does not improve vision,
SRF, nor alter the clinical course.130 The exact role of anti-
H. Pylori treatment in the management of CSCR remains to
be defined.
Methotrexate
Methotrexate is an antimetabolite drug that basically inhi-
bits folic acid metabolism. It is used successfully for treating
certain cancer entities, and some autoimmune rheumatologic
diseases, including certain forms of vasculitis. Kurup et al. ret-
rospectively evaluated methotrexate as a treatment for
chronic CSCR in 11 eyes. They found that the mean CMT
and visual acuity improved significantly compared to baseline
values, and 9 eyes (83%) remained dry after completion of
the treatment regimen. The mean duration of treatment
283
was 12 weeks.131 More trials are needed to explore the
potentials of methotrexate in treating CSCR and understand
its mechanism of action.
Search strategy
This review was conducted by performing an electronic
search of the Medline and EMBASE databases. The search
was limited to English language, and humans. We searched
the databases for relevant terms which included central ser-
ous retinopathy, central serous chorioretinopathy, photody-
namic therapy, CSC, CSCR, and treatment of central serous
chorioretinopathy. In addition, referenced articles from
extracted research papers were also reviewed for additional
data and the articles were retrieved if deemed relevant.
Conclusion
CSCR is a multifactorial disease that remains incompletely
understood. Recent imaging innovations have led to further
understanding and better monitoring of disease progression
and response to treatment. The gold standard of care for
CSCR is yet to be defined. To date, PDT offers good clinical
results that are maintained for an extended period of time.
Further long-term trials and continuous advances in retinal
therapeutics might culminate in achieving the drug of choice
for CSCR.
Conflict of interest
The authors declared that there is no conflict of interest.
Acknowledgment
The author would like to acknowledge Dr. Saba Al-
Rashaed, King Khaled Eye Specialist Hospital, for her kind
help with Fig. 1.
References
1. Von Graefe A. Ueber central recidivierende retinitis. Graefes Arch
Clin Exp Ophthalmol 1866;12:2115.
2. Yannuzzi LA, Shakin JL, Fisher YL, Altomonte MA. Peripheral retinal
detachments and retinal pigment epithelial atrophic tracts
secondary to central serous pigment epitheliopathy.
Ophthalmology 1984;91(12):155472.
3. Maumenee AE. Macular diseases: clinical manifestations. Trans Am
Acad Ophthalmol Otolaryngol 1965;69:60513.
4. Gass JD. Photocoagulation treatment of idiopathic central serous
choroidopathy. Trans Sect Ophthalmol Am Acad Ophthalmol
Otolaryngol 1977;83(3 Pt 1):45667.
5. Yannuzzi LA. Type A behavior and central serous chorioretinopathy.
Trans Am Ophthalmol Soc 1986;84:799845.
6. Gilbert CM, Owens SL, Smith PD, Fine SL. Long-term follow-up of
central serous chorioretinopathy. Br J Ophthalmol
1984;68(11):81520.
7. Yannuzzi LA. Type-A behavior and central serous chorioretinopathy.
Retina 1987;7(2):11131.
8. Prnte C, Flammer J. Choroidal capillary and venous congestion in
central serous chorioretinopathy. Am J Ophthalmol
1996;121(1):2634.
9. Polak BC, Baarsma GS, Snyers B. Diffuse retinal pigment
epitheliopathy complicating systemic corticosteroid treatment. Br
J Ophthalmol 1995;79(10):9225.
10. Wakakura M, Ishikawa S. Central serous chorioretinopathy
complicating systemic corticosteroid treatment. Br J Ophthalmol
1984;68(5):32931.
284
11. Harada T, Harada K. Six cases of central serous choroidopathy
induced by systemic corticosteroid therapy. Doc Ophthalmol
1985;60(1):3744.
12. Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, Kaiser-Kupfer
MI. Central serous chorioretinopathy in endogenous
hypercortisolism. Arch Ophthalmol 1993;111(9):122933.
13. Tittl MK, Spaide RF, Wong D, et al. Systemic findings associated
with central serous chorioretinopathy. Am J Ophthalmol
1999;128(1):638.
14. Trkc FM, Yksel H, Sahin A, et al. Effects of smoking on visual
acuity of central serous chorioretinopathy patients. Cutan Ocul
Toxicol 2014;33(2):1159. http://dx.doi.org/10.3109/
15569527.2013.810633.
15. Spaide RF, Campeas L, Haas A, et al. Central serous
chorioretinopathy in younger and older adults. Ophthalmology
1996;103(12):20709, discussion 207980.
16. Agarwal A. Gass atlas of macular diseases. 5th ed. Elsevier; 2011.
17. Desai UR, Alhalel AA, Campen TJ, Schiffman RM, Edwards PA,
Jacobsen GR. Central serous chorioretinopathy in African
Americans. J Natl Med Assoc 2003;95(7):5539.
18. Maruko I, Iida T, Ojima A, Sekiryu T. Subretinal dot-like precipitates
and yellow material in central serous chorioretinopathy. Retina
2011;31(4):75965. http://dx.doi.org/10.1097/
IAE.0b013e3181fbce8e.
19. Ie D, Yannuzzi LA, Spaide RF, Rabb MF, Blair NP, Daily MJ.
Subretinal exudative deposits in central serous chorioretinopathy. Br
J Ophthalmol 1993;77(6):34953.
20. Gass JD. Bullous retinal detachment. An unusual manifestation of
idiopathic central serous choroidopathy. Am J Ophthalmol
1973;75(5):81021.
21. OConnor PR. Multifocal serous choroidopathy. Ann Ophthalmol
1975;7(2):23745.
22. Bujarborua D, Nagpal PN, Deka M. Smokestack leak in central
serous chorioretinopathy. Graefes Arch Clin Exp Ophthalmol
2010;248(3):33951. http://dx.doi.org/10.1007/s00417-009-1212-5.
23. Spaide RF, Hall L, Haas A, et al. Indocyanine green
videoangiography of older patients with central serous
chorioretinopathy. Retina 1996;16(3):20313.
24. Iida T, Kishi S, Hagimura N, Shimizu K. Persistent and bilateral
choroidal vascular abnormalities in central serous chorioretinopathy.
Retina 1999;19(6):50812.
25. Imamura Y, Fujiwara T, Margolis R, Spaide RF. Enhanced depth
imaging optical coherence tomography of the choroid in central
serous chorioretinopathy. Retina 2009;29(10):146973. http://
dx.doi.org/10.1097/IAE.0b013e3181be0a83.
26. Okushiba U, Takeda M. Study of choroidal vascular lesions in central
serous chorioretinopathy using indocyanine green angiography.
Nihon Ganka Gakkai Zasshi 1997;101(1):7482.
27. Tittl M, Maar N, Polska E, Weigert G, Stur M, Schmetterer L.
Choroidal hemodynamic changes during isometric exercise in
patients with inactive central serous chorioretinopathy. Invest
Ophthalmol Vis Sci 2005;46(12):471721. http://dx.doi.org/
10.1167/iovs.05-0268.
28. Spitznas M. Pathogenesis of central serous retinopathy: a new
working hypothesis. Graefes Arch Clin Exp Ophthalmol
1986;224(4):3214.
29. Negi A, Marmor MF. Experimental serous retinal detachment and
focal pigment epithelial damage. Arch Ophthalmol
1984;102(3):4459.
30. Marmor MF. New hypotheses on the pathogenesis and treatment of
serous retinal detachment. Graefes Arch Clin Exp Ophthalmol
1988;226(6):54852.
31. Ryan S. Retina. 5th ed. Schachat A, Wilkinson C, Hinton D, Sadda S,
Wiedemann P, editors. Saunders; 2012. p. 1291305.
32. Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids
and catecholamines in the pathogenesis of central serous
chorioretinopathy: a rationale for new treatment strategies.
Ophthalmology 2002;109(10):17656.
33. Sakaue M, Hoffman BB. Glucocorticoids induce transcription
and expression of the alpha 1B adrenergic receptor gene in
DTT1 MF-2 smooth muscle cells. J Clin Invest 1991;88(2):
3859.
34. Hadcock JR, Malbon CC. Regulation of beta-adrenergic receptors
by permissive hormones: glucocorticoids increase steady-state
levels of receptor mRNA. Proc Natl Acad Sci USA
1988;85(22):84159.
M.A. Abouammoh
35. Zhao M, Clrier I, Bousquet E, et al. Mineralocorticoid receptor is
involved in rat and human ocular chorioretinopathy. J Clin Investig
2012;122(7):26729.
36. Ross A, Ross AH, Mohamed Q. Review and update of central serous
chorioretinopathy. Curr Opin Ophthalmol 2011;22(3):16673.
http://dx.doi.org/10.1097/ICU.0b013e3283459826.
37. Klein ML, Van Buskirk EM, Friedman E, Gragoudas E, Chandra S.
Experience with nontreatment of central serous choroidopathy.
Arch Ophthalmol 1974;91(4):24750.
38. Mudvari SS, Goff MJ, Fu AD, et al. The natural history of pigment
epithelial detachment associated with central serous
chorioretinopathy. Retina 2007;27(9):116873. http://dx.doi.org/
10.1097/IAE.0b013e318156db8a.
39. Aggio FB, Roisman L, Melo GB, Lavinsky D, Cardillo JA, Farah ME.
Clinical factors related to visual outcome in central serous
chorioretinopathy. Retina 2010;30(7):112834. http://dx.doi.org/
10.1097/IAE.0b013e3181cdf381.
40. Baran NV, Grl VP, Esgin H. Long-term macular function in eyes
with central serous chorioretinopathy. Clin Experiment Ophthalmol
2005;33(4):36972. http://dx.doi.org/10.1111/j.1442-
9071.2005.01027.x.
41. Bujarborua D. Long-term follow-up of idiopathic central serous
chorioretinopathy without laser. Acta Ophthalmol Scand
2001;79(4):41721.
42. Folk JC, Thompson HS, Han DP, Brown CK. Visual function
abnormalities in central serous retinopathy. Arch Ophthalmol
1984;102(9):1299302.
43. Koskela P, Laatikainen L, von Dickhoff K. Contrast sensitivity after
resolution of central serous retinopathy. Graefes Arch Clin Exp
Ophthalmol 1994;232(8):4736.
44. Maaranen TH, Tuppurainen KT, Mntyjrvi MI. Color vision defects
after central serous chorioretinopathy. Retina 2000;20(6):6337.
45. Levy J, Marcus M, Belfair N, Klemperer I, Lifshitz T. Central serous
chorioretinopathy in patients receiving systemic corticosteroid
therapy. Can J Ophthalmol 2005;40(2):21721. http://dx.doi.org/
10.1016/S0008-4182(05)80040-7.
46. Conrad R, Geiser F, Kleiman A, Zur B, Karpawitz-Godt A.
Temperament and character personality profile and illness-related
stress in central serous chorioretinopathy. Sci World J
2014;2014:631687. http://dx.doi.org/10.1155/2014/631687.
47. Sahin A, Bez Y, Kaya MC, Trkc FM, Sahin M, Yksel H. Psychological
distress and poor quality of life in patients with central serous
chorioretinopathy. Semin Ophthalmol 2014;29(2):736. http://
dx.doi.org/10.3109/08820538.2013.793728.
48. Yannuzzi LA. Central serous chorioretinopathy: a personal
perspective. Am J Ophthalmol 2010;149(3):3613. http://
dx.doi.org/10.1016/j.ajo.2009.11.017.
49. Mitsui Y, Matsubara M, Kanagawa M. Xenon light-exposure as a
treatment of central serous retinopathy (a preliminary report). Nihon
Ganka Kiyo 1969;20(3):2914.
50. Slusher MM. Krypton red laser photocoagulation in selected cases
of central serous chorioretinopathy. Retina 1986;6(2):814.
51. Novak MA, Singerman LJ, Rice TA. Krypton and argon laser
photocoagulation for central serous chorioretinopathy. Retina
1987;7(3):1629.
52. Robertson DM, Ilstrup D. Direct, indirect, and sham laser
photocoagulation in the management of central serous
chorioretinopathy. Am J Ophthalmol 1983;95(4):45766.
53. Leaver P, Williams C. Argon laser photocoagulation in the treatment
of central serous retinopathy. Br J Ophthalmol 1979;63(10):6747.
54. Ficker L, Vafidis G, While A, Leaver P. Long-term follow-up of a
prospective trial of argon laser photocoagulation in the treatment of
central serous retinopathy. Br J Ophthalmol 1988;72(11):82934.
55. Fok ACT, Chan PPM, Lam DSC, Lai TYY. Risk factors for recurrence
of serous macular detachment in untreated patients with central
serous chorioretinopathy. Ophthalmic Res 2011;46(3):1603. http://
dx.doi.org/10.1159/000324599.
56. Chen S-N, Hwang J-F, Tseng L-F, Lin C-J. Subthreshold diode
micropulse photocoagulation for the treatment of chronic central
serous chorioretinopathy with juxtafoveal leakage. Ophthalmology
2008;115(12):222934. http://dx.doi.org/10.1016/
j.ophtha.2008.08.026.
57. Lanzetta P, Furlan F, Morgante L, Veritti D, Bandello F. Nonvisible
subthreshold micropulse diode laser (810 nm) treatment of central
serous chorioretinopathy. A pilot study. Eur J Ophthalmol
2008;18(6):93440.
Advances in the treatment of CSCR
58. Gupta B, Elagouz M, McHugh D, Chong V, Sivaprasad S. Micropulse
diode laser photocoagulation for central serous chorio-retinopathy.
Clin Experiment Ophthalmol 2009;37(8):8015. http://dx.doi.org/
10.1111/j.1442-9071.2009.02157.x.
59. Ricci F, Missiroli F, Regine F, Grossi M, Dorin G. Indocyanine green
enhanced subthreshold diode-laser micropulse photocoagulation
treatment of chronic central serous chorioretinopathy. Graefes Arch
Clin Exp Ophthalmol 2009;247(5):597607. http://dx.doi.org/
10.1007/s00417-008-1014-1.
60. Verma L, Sinha R, Venkatesh P, Tewari HK. Comparative evaluation
of diode laser versus argon laser photocoagulation in patients with
central serous retinopathy: a pilot, randomized controlled trial
ISRCTN84128484. BMC Ophthalmol 2004;4:15. http://dx.doi.org/
10.1186/1471-2415-4-15.
61. Kawamura R, Ideta H, Hori H, et al. Transpupillary thermotherapy for
atypical central serous chorioretinopathy. Clin Ophthalmol
2012;6:1759. http://dx.doi.org/10.2147/OPTH.S28239.
62. Shukla D, Kolluru C, Vignesh TP, Karthikprakash S, Kim R.
Transpupillary thermotherapy for subfoveal leaks in central serous
chorioretinopathy. Eye (Lond) 2008;22(1):1006. http://dx.doi.org/
10.1038/sj.eye.6702449.
63. Hussain N, Khanna R, Hussain A, Das T. Transpupillary
thermotherapy for chronic central serous chorioretinopathy.
Graefes Arch Clin Exp Ophthalmol 2006;244(8):104551. http://
dx.doi.org/10.1007/s00417-005-0175-4.
64. Giudice GLo, de Belvis V, Tavolato M, Galan A. Large-spot
subthreshold transpupillary thermotherapy for chronic serous
macular detachment. Clin Ophthalmol 2011;5:35560. http://
dx.doi.org/10.2147/OPTH.S16014.
65. Chan W-M, Lai TYY, Lai RYK, Liu DTL, Lam DSC. Half-dose
verteporfin photodynamic therapy for acute central serous
chorioretinopathy: one-year results of a randomized controlled
trial. Ophthalmology 2008;115(10):175665. http://dx.doi.org/
10.1016/j.ophtha.2008.04.014.
66. Schmidt-Erfurth U, Laqua H, Schltzer-Schrehard U, Viestenz A,
Naumann GOH. Histopathological changes following photodynamic
therapy in human eyes. Arch Ophthalmol 2002;120(6):83544.
67. Tarantola RM, Law JC, Recchia FM, Sternberg P, Agarwal A.
Photodynamic therapy as treatment of chronic idiopathic central
serous chorioretinopathy. Lasers Surg Med 2008;40(10):6715.
http://dx.doi.org/10.1002/lsm.20720.
68. Chan W-M, Lam DSC, Lai TYY, Tam B, Liu DTL, Chan CKM.
Choroidal vascular remodelling in central serous chorioretinopathy
after indocyanine green guided photodynamic therapy with
verteporfin: a novel treatment at the primary disease level. Br J
Ophthalmol 2003;87:14539.
69. Inoue R, Sawa M, Tsujikawa M, Gomi F. Association between the
efficacy of photodynamic therapy and indocyanine green angiography
findings for central serous chorioretinopathy. Am J Ophthalmol
2010;149(3):441-6.e1-2. http://dx.doi.org/10.1016/j.ajo.2009.10.011.
70. Moon JW, Yu HG, Kim TW, Kim HC, Chung H. Prognostic factors
related to photodynamic therapy for central serous
chorioretinopathy. Graefes Arch Clin Exp Ophthalmol
2009;247(10):131523. http://dx.doi.org/10.1007/s00417-009-
1104-8.
71. Tsakonas GD, Kotsolis AI, Koutsandrea C, Georgalas I,
Papaconstantinou D, Ladas ID. Multiple spots of photodynamic
therapy for the treatment of severe chronic central serous
chorioretinopathy. Clin Ophthalmol 2012;6:163944. http://
dx.doi.org/10.2147/OPTH.S35733.
72. Ruiz-Moreno JM, Lugo FL, Armad F, et al. Photodynamic therapy
for chronic central serous chorioretinopathy. Acta Ophthalmol
2010;88(3):3716. http://dx.doi.org/10.1111/j.1755-
3768.2008.01408.x.
73. Copete S, Ruiz-Moreno JM, Cava C, Montero JA. Retinal thickness
changes following photodynamic therapy in chronic central serous
chorioretinopathy. Graefes Arch Clin Exp Ophthalmol
2012;250(6):8038. http://dx.doi.org/10.1007/s00417-011-1900-9.
74. Vasconcelos H, Marques I, Santos AR. Long-term chorioretinal
changes after photodynamic therapy for chronic central serous
chorioretinopathy. Graefes Arch Clin Exp Ophthalmol 2013;251(7):
1697705. http://dx.doi.org/10.1007/s00417-013-2270-2.
75. Lee PY, Kim KS, Lee WK. Severe choroidal ischemia following
photodynamic therapy for pigment epithelial detachment and
chronic central serous chorioretinopathy. Jpn J Ophthalmol
2009;53(1):526. http://dx.doi.org/10.1007/s10384-008-0613-z.
285
76. Reibaldi M, Cardascia N, Longo A, et al. Standard-fluence versus
low-fluence photodynamic therapy in chronic central serous
chorioretinopathy: a nonrandomized clinical trial. Am J
Ophthalmol 2010;149(2):307-315.e2. http://dx.doi.org/10.1016/
j.ajo.2009.08.026.
77. Lai TYY, Chan W-M, Li H, Lai RYK, Liu DTL, Lam DSC. Safety
enhanced photodynamic therapy with half dose verteporfin for
chronic central serous chorioretinopathy: a short term pilot study. Br
J Ophthalmol 2006;90(7):86974. http://dx.doi.org/10.1136/
bjo.2006.090282.
78. Kim S-W, Oh J, Oh IK, Huh K. Retinal pigment epithelial tear after
half fluence PDT for serous pigment epithelial detachment in central
serous chorioretinopathy. Ophthalmic Surg Lasers Imag
2009;40(3):3003.
79. Lim JW, Kang SW, Kim Y-T, Chung SE, Lee SW. Comparative study
of patients with central serous chorioretinopathy undergoing focal
laser photocoagulation or photodynamic therapy. Br J Ophthalmol
2011;95(4):5147. http://dx.doi.org/10.1136/bjo.2010.182121.
80. Kim KS, Lee WK, Lee SB. Half-dose photodynamic therapy targeting
the leakage point on the fluorescein angiography in acute central
serous chorioretinopathy: a pilot study. Am J Ophthalmol
2014;157(2):366-373.e1. http://dx.doi.org/10.1016/
j.ajo.2013.10.013.
81. Maruko I, Iida T, Sugano Y, Ojima A, Ogasawara M, Spaide RF.
Subfoveal choroidal thickness after treatment of central serous
chorioretinopathy. Ophthalmology 2010;117(9):17929. http://
dx.doi.org/10.1016/j.ophtha.2010.01.023.
82. Ratanasukon M, Thongthong K, Bhurayanontachai P,
Jirarattanasopa P. Photoreceptor disruption in central serous
chorioretinopathy treated by half-dose photodynamic therapy.
Clin Ophthalmol 2013;7:8792. http://dx.doi.org/10.2147/
OPTH.S39584.
83. Karakus SH, Basarir B, Pinarci EY, Kirandi EU, Demirok A. Long-term
results of half-dose photodynamic therapy for chronic central serous
chorioretinopathy with contrast sensitivity changes. Eye (Lond)
2013;27(5):61220. http://dx.doi.org/10.1038/eye.2013.24.
84. Dang Y, Sun X, Xu Y, et al. Subfoveal choroidal thickness after
photodynamic therapy in patients with acute idiopathic central
serous chorioretinopathy. Ther Clin Risk Manage 2014;10:3743.
http://dx.doi.org/10.2147/TCRM.S54213.
85. Zhao M-W, Zhou P, Xiao H-X, et al. Photodynamic therapy for acute
central serous chorioretinopathy: the safe effective lowest dose of
verteporfin. Retina 2009;29(8):115561. http://dx.doi.org/10.1097/
IAE.0b013e3181a6c028.
86. Uetani R, Ito Y, Oiwa K, Ishikawa K, Terasaki H. Half-dose vs one-
third-dose photodynamic therapy for chronic central serous
chorioretinopathy. Eye (Lond) 2012;26(5):6409. http://dx.doi.org/
10.1038/eye.2012.66.
87. Nicol M, Zoli D, Musolino M, Traverso CE. Association between the
efficacy of half-dose photodynamic therapy with indocyanine green
angiography and optical coherence tomography findings in the
treatment of central serous chorioretinopathy. Am J Ophthalmol
2012;153(3):474-480.e1. http://dx.doi.org/10.1016/
j.ajo.2011.08.015.
88. Alcubierre R, Arias L, Lorenzo D, Pujol O, Rubio M. Low-fluence
photodynamic therapy in chronic central serous chorioretinopathy.
Arch la Soc Espaola Oftalmol 2012;87(1):38. http://dx.doi.org/
10.1016/j.oftale.2012.04.006, English Ed..
89. Butler AL, Fung AT, Merkur AB, Albiani DA, Forooghian F. Very
minimal fluence photodynamic therapy for chronic central serous
chorioretinopathy. Can J Ophthalmol 2012;47(1):424. http://
dx.doi.org/10.1016/j.jcjo.2011.12.020.
90. Bae SH, Heo JW, Kim C, et al. A randomized pilot study of low-
fluence photodynamic therapy versus intravitreal ranibizumab for
chronic central serous chorioretinopathy. Am J Ophthalmol
2011;152(5):784-92.e2. http://dx.doi.org/10.1016/
j.ajo.2011.04.008.
91. Lee T-G, Kim JE. Photodynamic therapy for steroid-associated
central serous chorioretinopathy. Br J Ophthalmol
2011;95(4):51823. http://dx.doi.org/10.1136/bjo.2010.181149.
92. Ohkuma Y, Hayashi T, Sakai T, Watanabe A, Tsuneoka H. One-year
results of reduced fluence photodynamic therapy for central serous
chorioretinopathy: the outer nuclear layer thickness is associated
with visual prognosis. Graefes Arch Clin Exp Ophthalmol
2013;251(8):190917. http://dx.doi.org/10.1007/s00417-013-2289-
4.
286
93. Kang NH, Kim YT. Change in subfoveal choroidal thickness in central
serous chorioretinopathy following spontaneous resolution and low-
fluence photodynamic therapy. Eye (Lond) 2013;27(3):38791.
http://dx.doi.org/10.1038/eye.2012.273.
94. Nicol M, Eandi CM, Alovisi C, et al. Half-fluence versus half-dose
photodynamic therapy in chronic central serous chorioretinopathy.
Am J Ophthalmol 2014;157(5):10337. http://dx.doi.org/10.1016/
j.ajo.2014.01.022.
95. Seong HK, Bae JH, Kim ES, Han JR, Nam WH, Kim HK. Intravitreal
bevacizumab to treat acute central serous chorioretinopathy: short-
term effect. Ophthalmologica 2009;223(5):3437. http://dx.doi.org/
10.1159/000224782.
96. Schaal KB, Hoeh AE, Scheuerle A, Schuett F, Dithmar S. Intravitreal
bevacizumab for treatment of chronic central serous
chorioretinopathy. Eur J Ophthalmol 2009;19(4):6137.
97. Lim JW, Kim MU, Shin M-C. Aqueous humor and plasma levels of
vascular endothelial growth factor and interleukin-8 in patients with
central serous chorioretinopathy. Retina 2010;30(9):146571. http://
dx.doi.org/10.1097/IAE.0b013e3181d8e7fe.
98. Shin MC, Lim JW. Concentration of cytokines in the aqueous humor
of patients with central serous chorioretinopathy. Retina 2011;31(9):
193743. http://dx.doi.org/10.1097/IAE.0b013e31820a6a17.
99. Jung SH, Kim K-A, Sohn SW, Yang SJ. Cytokine levels of the
aqueous humour in central serous chorioretinopathy. Clin Exp
Optom 2014;97(3):2649. http://dx.doi.org/10.1111/cxo.12125.
100. Bae SH, Heo J, Kim C, et al. Low-fluence photodynamic therapy
versus ranibizumab for chronic central serous chorioretinopathy:
one-year results of a randomized trial. Ophthalmology
2014;121(2):55865. http://dx.doi.org/10.1016/
j.ophtha.2013.09.024.
101. Lim SJ, Roh MI, Kwon OW. Intravitreal bevacizumab injection for
central serous chorioretinopathy. Retina 2010;30(1):1006. http://
dx.doi.org/10.1097/IAE.0b013e3181bcf0b4.
102. Arevalo JF, Espinoza JV. Single-session combined photodynamic
therapy with verteporfin and intravitreal anti-vascular endothelial
growth factor therapy for chronic central serous chorioretinopathy:
a pilot study at 12-month follow-up. Graefes Arch Clin Exp
Ophthalmol 2011;249(8):115966. http://dx.doi.org/10.1007/
s00417-011-1651-7.
103. Aydin E. The efficacy of intravitreal bevacizumab for acute central
serous chorioretinopathy. J Ocul Pharmacol Ther 2013;29(1):103.
http://dx.doi.org/10.1089/jop.2012.0072.
104. Semeraro F, Romano MR, Danzi P, Morescalchi F, Costagliola C.
Intravitreal bevacizumab versus low-fluence photodynamic therapy
for treatment of chronic central serous chorioretinopathy. Jpn J
Ophthalmol 2012;56(6):60812. http://dx.doi.org/10.1007/s10384-
012-0162-3.
105. Lee ST, Adelman RA. The treatment of recurrent central serous
chorioretinopathy with intravitreal bevacizumab. J Ocul Pharmacol
Ther 2011;27(6):6114. http://dx.doi.org/10.1089/jop.2011.0045.
106. Torres-Soriano ME, Garca-Aguirre G, Kon-Jara V, et al. A pilot
study of intravitreal bevacizumab for the treatment of central serous
chorioretinopathy (case reports). Graefes Arch Clin Exp Ophthalmol
2008;246(9):12359. http://dx.doi.org/10.1007/s00417-008-0856-x.
107. Lim JW, Kim MU. The efficacy of intravitreal bevacizumab for
idiopathic central serous chorioretinopathy. Graefes Arch Clin Exp
Ophthalmol 2011;249(7):96974. http://dx.doi.org/10.1007/
s00417-010-1581-9.
108. Montero JA, Ruiz-Moreno JM, Fernandez-Muoz M. Intravitreal
bevacizumab to treat choroidal neovascularization following
photodynamic therapy in central serous choroidopathy. Eur J
Ophthalmol 21(4): 5035. doi: http://dx.doi.org/10.5301/EJO.
2011.6290.
109. Chan W-M, Lai TYY, Liu DTL, Lam DSC. Intravitreal bevacizumab
(avastin) for choroidal neovascularization secondary to central
serous chorioretinopathy, secondary to punctate inner
choroidopathy, or of idiopathic origin. Am J Ophthalmol
2007;143(6):97783. http://dx.doi.org/10.1016/j.ajo.2007.02.039.
110. Meyerle CB, Freund KB, Bhatnagar P, Shah V, Yannuzzi LA.
Ketoconazole in the treatment of chronic idiopathic central serous
chorioretinopathy. Retina 2007;27(7):9436. http://dx.doi.org/
10.1097/IAE.0b013e318050ca69.
111. Golshahi A, Klingmller D, Holz FG, Eter N. Ketoconazole in the
treatment of central serous chorioretinopathy: a pilot study. Acta
Ophthalmol 2010;88(5):57681. http://dx.doi.org/10.1111/j.1755-
3768.2008.01467.x.
M.A. Abouammoh
112. Nielsen JS, Jampol LM. Oral mifepristone for chronic central serous
chorioretinopathy. Retina 2011;31(9):192836. http://dx.doi.org/
10.1097/IAE.0b013e31821c3ef6.
113. Bousquet E, Beydoun T, Zhao M, Hassan L, Offret O, Behar-Cohen
F. Mineralocorticoid receptor antagonism in the treatment of
chronic central serous chorioretinopathy: a pilot study. Retina
2013;33(10):2096102. http://dx.doi.org/10.1097/
IAE.0b013e318297a07a.
114. Maier M, Stumpfe S, Feucht N, Strobl P, Rath V, Lohmann CP.
Mineralocorticoid receptor antagonists as treatment option for
acute and chronic central serous chorioretinopathy. Ophthalmologe
2014;111(2):17380. http://dx.doi.org/10.1007/s00347-013-3001-
0.
115. Breukink MB, den Hollander AI, Keunen JEE, Boon CJF, Hoyng CB.
The use of eplerenone in therapy-resistant chronic central serous
chorioretinopathy. Acta Ophthalmol 2014. http://dx.doi.org/
10.1111/aos.12392.
116. Gruszka A. Potential involvement of mineralocorticoid receptor
activation in the pathogenesis of central serous chorioretinopathy:
case report. Eur Rev Med Pharmacol Sci 2013;17(10):136973.
117. Steinle NC, Gupta N, Yuan A, Singh RP. Oral rifampin utilisation for
the treatment of chronic multifocal central serous retinopathy. Br J
Ophthalmol 2012;96(1):103. http://dx.doi.org/10.1136/
bjophthalmol-2011-300183.
118. Ravage ZB, Packo KH, Creticos CM, Merrill PT. Chronic central
serous chorioretinopathy responsive to rifampin. Retin Cases Br Rep
2012;6(1):12932.
119. Nelson J, Saggau DD, Nielsen JS. Rifampin induced hepatotoxicity
during treatment for chronic central serous chorioretinopathy. Retin
Cases Br Rep 2014;8(1):702.
120. Forooghian F, Meleth AD, Cukras C, Chew EY, Wong WT, Meyerle
CB. Finasteride for chronic central serous chorioretinopathy. Retina
2011;31(4):76671. http://dx.doi.org/10.1097/
IAE.0b013e3181f04a35.
121. Tatham A, Macfarlane A. The use of propranolol to treat central
serous chorioretinopathy: an evaluation by serial OCT. J Ocul
Pharmacol Ther 2006;22(2):1459. http://dx.doi.org/10.1089/
jop.2006.22.145.
122. Avci R, Deutman AF. Treatment of central serous choroidopathy
with the beta receptor blocker metoprolol (preliminary results). Klin
Monbl Augenheilkd 1993;202(3):199205. http://dx.doi.org/
10.1055/s-2008-1045583.
123. Chrapek O, Jirkova B, Kandrnal V, Rehak J, Sin M. Treatment of
central serous chorioretinopathy with beta-blocker metipranolol.
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
2013;36. http://dx.doi.org/10.5507/bp.2013.015.
124. Pikkel J, Beiran I, Ophir A, Miller B. Acetazolamide for central serous
retinopathy. Ophthalmology 2002;109(9):17235.
125. Caccavale A, Imparato M, Romanazzi F, Negri A, Porta A, Ferentini
F. A new strategy of treatment with low-dosage acetyl salicylic acid
in patients affected by central serous chorioretinopathy. Med
Hypotheses 2009;73(3):4357. http://dx.doi.org/10.1016/
j.mehy.2009.03.036.
126. Caccavale A, Romanazzi F, Imparato M, Negri A, Morano A,
Ferentini F. Low-dose aspirin as treatment for central serous
chorioretinopathy. Clin Ophthalmol 2010;4:899903.
127. Giusti C, Mauget-Fasse M. Helicobacter pylori and
idiopathic central serous chorioretinopathy. Swiss Med Wkly
2004;134(2728):3958.
128. Giusti C. Association of Helicobacter pylori with central serous
chorioretinopathy: hypotheses regarding pathogenesis. Med
Hypotheses 2004;63(3):5247. http://dx.doi.org/10.1016/
j.mehy.2004.02.020.
129. Rahbani-Nobar MB, Javadzadeh A, Ghojazadeh L, Rafeey M,
Ghorbanihaghjo A. The effect of Helicobacter pylori treatment on
remission of idiopathic central serous chorioretinopathy. Mol Vis
2011;17(January):99103.
130. Dang Y, Mu Y, Zhao M, Li L, Guo Y, Zhu Y. The effect of eradicating
Helicobacter pylori on idiopathic central serous chorioretinopathy
patients. Ther Clin Risk Manage 2013;9:35560. http://dx.doi.org/
10.2147/TCRM.S50407.
131. Kurup SK, Oliver A, Emanuelli A, Hau V, Callanan D. Low-dose
methotrexate for the treatment of chronic central serous
chorioretinopathy: a retrospective analysis. Retina
2012;32(10):2096101. http://dx.doi.org/10.1097/
IAE.0b013e31825dd281.